Doyle Caroline, Swain Walker A, Swain Ewald Holly A, Ewald Paul W
Department of Biology, Bellarmine University, Louisville, KY 40205, USA.
Department of Lifelong Education, Administration, and Policy, University of Georgia, Athens, GA 30602, USA.
Evol Hum Sci. 2019 Dec 9;1:e14. doi: 10.1017/ehs.2019.15. eCollection 2019.
The evolutionary basis for clinical depression is not well understood. A growing body of literature that is not based on evolutionary logic links inflammation to depression. Integration of these findings with an evolutionary framework for depression, however, needs to address the reasons why the body's inflammatory response would be regulated so poorly that it would result in incapacitating depression. Pathogen induction of inflammation offers an explanation, but the extent to which the association between inflammation and depression can be attributed to general inflammation as opposed to particular effects of pro-inflammatory pathogens remains unclear. This paper reports a study of sexually transmitted pathogens, which addresses this issue. Although several sexually transmitted pathogens were associated with depression according to bivariate tests, only and were significantly associated with depression by a multivariate analysis that accounted for correlations among the pathogens. This finding is consistent with the hypothesis that infection may contribute to depression through induction of tryptophan restriction, and a consequent depletion of serotonin. It reinforces the idea that some depression may be caused by specific pathogens in specific evolutionary arms races with their human host.
临床抑郁症的进化基础尚未得到很好的理解。越来越多并非基于进化逻辑的文献将炎症与抑郁症联系起来。然而，要将这些发现与抑郁症的进化框架相结合，就需要探讨为何身体的炎症反应调控得如此糟糕，以至于会导致使人丧失能力的抑郁症。病原体引发炎症提供了一种解释，但炎症与抑郁症之间的关联在多大程度上可归因于一般性炎症，而非促炎性病原体的特定影响，仍不明确。本文报告了一项关于性传播病原体的研究，该研究解决了这一问题。尽管根据双变量检验，几种性传播病原体与抑郁症有关联，但在考虑了病原体之间相关性的多变量分析中，只有[具体病原体1]和[具体病原体2]与抑郁症有显著关联。这一发现与感染可能通过诱导色氨酸限制从而导致血清素耗竭进而引发抑郁症的假说相一致。它强化了这样一种观点，即某些抑郁症可能是由特定病原体在与人类宿主的特定进化军备竞赛中导致的。
